Mototsugu Ninomiya

Long-Term Right Ventricular Volume Overload Increases Myocardial Fluorodeoxyglucose Uptake in the Interventricular Septum in Patients With Atrial Septal Defect

BACKGROUND Several studies have shown that long-term right ventricular (RV) overload in animal models alters myocardial energy substrate metabolism. However, whether long-term RV volume overload alters this metabolism in the human is unclear. METHODS AND RESULTS We performed positron emission tomography with [(18)F]fluorodeoxyglucose (FDG) and single-photon emission tomography (SPECT) with [(201)Tl]TlCl (Tl) and [(123)I]15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid (BMIPP) in 11 patients with atrial septal defect (ASD) and 11 control subjects. In the FDG study, we calculated myocardial metabolic rate of glucose (MMR) in interventricular septum (IVS) and left ventricular (LV) free wall. MMR was significantly increased in IVS compared with LV free wall in the ASD patients (420+/-35 versus 333+/-32 mol x kg(-1) x min(-1); P<0.05) but not in the control group (347+/-27 versus 357+/-25 mol x kg(-1) x min(-1)). In both ASD and control groups, SPECT count was not significantly different between IVS and LV free wall in Tl (ASD, 160+/-11 versus 177+/-12; control, 141+/-12 versus 157+/-14 counts per 15 minutes) and BMIPP studies (ASD, 203+/-14 versus 212+/-18; control, 162+/-16 versus 176+/-16 counts per 15 minutes). MMR in the IVS/LV free wall ratio in the ASD group significantly correlated with indices related to RV volume overload. CONCLUSIONS Given the assumption that long-term RV volume overload did not affect the lumped constant, the present study suggests that, unlike myocardial perfusion or fatty acid analogue uptake, myocardial glucose utilization in IVS relative to LV free wall is increased in relation to long-term RV volume overload in patients with ASD.

Nonselective endothelin receptor antagonist initiated soon after the onset of myocardial infarction may deteriorate 24-hour survival.

&NA; To investigate the effects of endothelin blockade initiated immediately after the onset of myocardial infarction on survival and left ventricular remodeling, treatment with the nonselective receptor antagonist TAK‐044 (n = 22) or saline (n = 19) for 3 weeks was initiated immediately after coronary ligation in rats. The 24‐h survival rate was significantly lower in the TAK‐044 group than in the saline group. The systolic blood pressure 24 h after the onset of myocardial infarction was similar in the saline and TAK‐044 groups, although it was significantly lower in the TAK‐044 group during the 3‐week protocol. Heart weight/tibial length was significantly increased in the TAK‐044 group compared with the saline group. As all deaths in the TAK‐044 group occurred within 24 h after myocardial infarction, we performed additional experiments using a separate group of rats 12–16 h after myocardial infarction. Plasma and myocardial endothelin‐1 levels were significantly increased, and a bolus injection of TAK‐044 significantly reduced left ventricular dP/dtmax in these rats that had had a myocardial infarction compared with sham‐operated rats. Endothelin receptor blockade initiated immediately after the onset of myocardial infarction may deteriorate acute‐phase survival and left ventricular remodeling. Inhibition of the positive inotropic action of endothlin‐1 may partially explain the increased 24‐h mortality.

Diverticulum of the superior vena cava

A 14-year-old girl underwent operation with the diagnosis of diverticulum of the superior vena cava. Microscopic findings revealed a diverticulum with venous architecture. This represents a rare case of a giant diverticulum of the superior vena cava.

Should increasing the dose or adding an AT1 receptor blocker follow a relatively low dose of ACE inhibitor initiated in acute myocardial infarction

OBJECTIVE Based on currently available clinical evidence, we should use high-dose angiotensin converting enzyme inhibitor (ACE-I) for patients with acute myocardial infarction (MI), initiating it at incremental doses to avoid excessive hypotension. Recent animal studies with acute MI models failed to demonstrate the superiority of the combination therapy of ACE-I and angiotensin receptor blocker (ARB) to high-dose ACE-I treatment with comparable blood pressure reductions, which however might be attributed to the initiation of the targeted doses from the beginning. The aim of this study was to compare the effect of increasing the dose of ACE-I with that of adding ARB following a relatively low dose of ACE-I on the survival and left ventricular (LV) remodeling after MI. METHODS Rats underwent left coronary artery ligation and were treated with either ACE-I temocapril (5 mg/kg/day) or vehicle for 2 weeks, which was initiated 3 days after the surgery. The rats treated with temocapril were further randomly assigned to receive either high-dose temocapril (10 mg/kg/day) or combination therapy (temocapril 5 mg/kg/day+olmesartan 2.5 mg/kg/day), which was continued for another 6 weeks. RESULTS Both treatments similarly reduced the blood pressure, improved survival and ameliorated LV enlargement. In contrast, several parameters of LV function were significantly ameliorated only by the high-dose ACE-I but not by the combination therapy. CONCLUSIONS After the initiation of a relatively low dose of ACE-I in acute MI, increasing the dose of ACE-I or adding ARB may equally improve survival and LV remodeling in the setting of an equal hypotensive effect. Further study with a longer treatment protocol is required to determine whether the several favorable effects on LV function elicited only by the high-dose ACE-I treatment provide further beneficial effects on survival and LV remodeling compared with the combination therapy.

Different responses of left ventricular systolic function to changes in right ventricular volume and shortening —comparison between aorto-femoral vein and aorto-left atrium shunts in dog hearts

SummaryIt has been reported that left ventricular end-systolic volume decreases during arteriovenous shunt and increases during subclavian artery-left atrium shunt at a constant end-systolic pressure. The mechanism of the opposing changes in end-systolic volume during the two types of shunt is not clear. One possible cause is that left ventricular pump function with enhanced right ventricular ejection differs from that without enhancement. To investigate this hypothesis, we studied the two types of shunt (Aorto-femoral vein shunt, AoFV; aorto-left atrium shunt, AoLA) with matched reduction of systemic vascular resistance in open-chest dogs with β-blockade. Both right and left ventricular volumes and shortenings were assessed from short-axis views by two-dimensional (2D)-echocardiogram. Left ventricular end-systolic short-axis area decreased from 76 ± 3 to 62 ± 3% in AoFV shunt (p < 0.05), but tended to increase in AoLA shunt (76 ± 4 in control state vs 81 ± 5% in AoLA, NS) in spite of a similar reduction in left ventricular end-systolic pressure. There was no difference in left ventricular shortening, but significant differences were observed in right ventricular shortening (50 ± 8 in AoFV vs 24 ± 7% in AoLA, p < 0.05) and right ventricular short-axis area at end-diastole (142 ± 6 in AoFV vs 96 ± 3% in AoLA, p < 0.01), and at end-systole (92 ± 8 in AoFV vs 73 ± 7% in AoLA, p < 0.05) between the two types of shunt. We conclude that the different changes in left ventricular end-systolic short-axis area found in the two shunts are not caused by the different left ventricular shortenings, but by the different right ventricular mechanical actions. These findings suggest that left ventricular pumping action in the high output state changes, depending on whether it is accompanied by augmented ejection of the right ventricle or not.